migraine pathology: Migraines are thought to be caused by the release of peptide neurotransmitters (primarily the calcitonin gene-related peptide, viz. CGRP) from the trigeminal nerve distribution into the intracranial arteries. These neurotransmitters are known to be powerful vasodilators resulting in cranial vasodilation. This may further lead to extravasation of blood plasma and plasma proteins resulting in perivascular oedema. Perivascular oedema can cause mechanical stretching, leading to activation of pain nerve endings in the dura which may be the cause of the painful headache associated with migraines.

migraine treatment:

• ergot alkaloids: eg. Ergonovine. Partial agonist at 5-HT and at alpha-adrenoreceptors especially in vessels thereby preventing the vasodilation associated with migraines.
• triptans: eg. sumatriptan. Selective agonists for 5-HT1D and 5-HT1B: this causes vasoconstriction and prevents the vasodilatory effects of the migraine as well as the pain associated with it, they also modulate neurotransmitter release thus reducing the amount of CGRP.
• anti-inflammatory analgesics (NSAIDs): eg. asprin. Effective in pain management of pain associated with migraines.
• beta-blockers: eg. propanolol. Effective in the prophylaxis of migraine.
• anticonvulsants: eg.topiramate, valproic acid. Used in the prophylactic treatment of migraines.
• calcium-channel blockers: eg. verapamil, flunarizine. Effective in the prophylaxis of migraine.